
doi: 10.3892/ijo.18.3.549
pmid: 11179485
The p51 gene encodes a protein with significant homology to p53, thus, it is a candidate tumor suppressor gene. To investigate the involvement of the p51 gene in human ovarian carcinogenesis, p51 gene alterations were examined in primary ovarian cancers and ovarian cancer cell lines. Mutation analysis of the p51 gene was performed in 40 primary ovarian cancers and 6 ovarian cancer cell lines using the PCR-SSCP and direct sequencing methods. Expression of p51 mRNA was examined in 9 primary ovarian cancers and 5 ovarian cancer cell lines by Northern blot and RT-PCR analyses. No mutations of the p51 gene causing amino acid substitutions or frameshifts were detected in either primary tumors or cancer cell lines by PCR-SSCP analysis of the entire coding region, although several genetic polymorphisms were detected in three samples. Allelic imbalance was detected in 3 of 19 (16%) primary ovarian cancers. No p51 gene expression was detected in 9 primary ovarian cancers and the corresponding normal ovarian tissues by Northern blot and by RT-PCR analyses. One of 5 ovarian cancer cell lines showed p51 gene expression by Northern blot analysis (20%). These results indicated that p51 gene expression was silent in normal ovarian tissues and primary ovarian cancers, and that mutation of the p51 gene does not play a major role in the development of ovarian cancer.
Ovarian Neoplasms, Polymorphism, Genetic, Reverse Transcriptase Polymerase Chain Reaction, DNA, Exons, Sequence Analysis, DNA, Blotting, Northern, Phosphoproteins, Introns, DNA-Binding Proteins, Mutation, Trans-Activators, Tumor Cells, Cultured, Humans, Female, Genes, Tumor Suppressor, RNA, Messenger, Polymorphism, Single-Stranded Conformational, DNA Primers, Transcription Factors
Ovarian Neoplasms, Polymorphism, Genetic, Reverse Transcriptase Polymerase Chain Reaction, DNA, Exons, Sequence Analysis, DNA, Blotting, Northern, Phosphoproteins, Introns, DNA-Binding Proteins, Mutation, Trans-Activators, Tumor Cells, Cultured, Humans, Female, Genes, Tumor Suppressor, RNA, Messenger, Polymorphism, Single-Stranded Conformational, DNA Primers, Transcription Factors
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